Cases reported "Coma"

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1/7. Adrenal crisis presenting as hypoglycemic coma.

    An 18-month-old male infant presented with hypoglycemic coma and clinical signs of bronchopneumonia. He was suspected of suffering from septic shock. The patient progressed to irreversible multiple organ failure before the diagnosis of adrenal crisis was established. plasma levels of ACTH and cortisol remained undetectable. renin and aldosterone were normal. An autopsy failed to demonstrate any adrenal gland cortical tissue. Immunohistochemical staining demonstrated the presence of all pituitary hormones except ACTH, establishing the diagnosis of isolated ACTH deficiency. intensive care clinicians should consider adrenal crisis in non-diabetic children with hypoglycemia and rapid circulatory deterioration.
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2/7. coma blisters in a case of fatal theophylline intoxication.

    A case of fatal poisoning caused by theophylline toxicity (serum level 127 micro g/ml) is presented. At external examination, skin blisters on regions exposed to pressure were distinctive. Histologic examination demonstrated subepidermal bullae with eosinophilic necrosis of the eccrine sweat gland coil but no epidermal necrosis, vascular changes, or inflammatory infiltrate. To the authors' knowledge, this is the first description of coma blisters in a case of theophylline intoxication.
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3/7. Hyponatraemic coma induced by desmopressin and ibuprofen in a woman with von Willebrand's disease.

    A middle-aged woman was admitted to the hospital after being found unconscious at home. A brain CT scan excluded an intracranial bleed or other focal abnormality. Laboratory analysis showed hyponatraemia (sodium: 121 mmol L(-1)) and a low plasma osmolality, with normal sodium excretion and urine osmolality. A diagnosis of hyponatraemic coma was made. The patient was treated with water restriction; 24 h later the sodium was 135 mmol L(-1) and the patient was neurologically fully recovered. The patient, who suffered from von Willebrand's disease, had received desmopressin and ibuprofen for analgesia 2 days before after a dental intervention. She had received desmopressin several times in the past without any complications. A few patients treated with desmopressin for coagulation abnormalities have been reported to develop water intoxication and severe hyponatraemia resulting in seizures and coma. By inhibiting prostaglandin synthesis, non-steroid anti-inflammatory agents (NSAIDs) potentiate the effect of water reabsorption in the renal tubules of vasopressin, therefore enhancing water retention. Desmopressin and NSAIDs should not be used in combination in patients with bleeding disorders, but it is often followed in clinical practice. In addition, this is probably not an unusual situation in patients treated with desmopressin for other 'non-haemorrhagic' indications. This report emphasizes the need for practitioners to be aware of this rare but severe complication.
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4/7. Drug-induced sweat gland necrosis in a non-comatose patient: a case presentation.

    BACKGROUND: coma-induced bullae and sweat gland necrosis is a rare clinicopathological entity often associated with drug-induced coma. SUBJECT: We report a case with clinical and histopathologic findings characteristic of blisters and sweat gland necrosis occurring in a non-comatose patient. CONCLUSIONS: skin blisters with underlying sweat gland necrosis is an entity previously reported to occur in comatose patients, our findings open new questions about the role of the drugs in the pathogenesis of those conditions.
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5/7. Multiple bullae and paresis after drug-induced coma.

    Two cases of bullous skin lesions and paresis following coma due to the ingestion of many antipsychotic drugs were reported. Histological examination showed an intra-epidermal blister in case 1 and degeneration of sweat glands in both cases. An immunofluorescence study showed massive deposits of IgM and C3 in the dermal vessels. As similar deposits of immunoglobulin and complement were not observed in patients with ordinary lesions such as decubitus, a different mechanism in the formation of the bullous skin lesion other than pressure is suggested.
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6/7. diazepam-induced coma with bullae and eccrine sweat gland necrosis.

    Bullous skin lesions that indicate sweat gland necrosis have been known to occur in drug-induced coma resulting from barbiturates and in carbon monoxide poisoning. To our knowledge, this is the first cases in which diazepam is implicated in causing bullous lesions over pressure points, and the first case showing on biopsy specimen eccrine sweat gland and sweat duct necrosis. Penile and oral lesions are being described here for the first time to our knowledge. The following mechanisms could be responsible for the skin lesions: hypoxia, local pressure, hyperthermia with excessive sweating, and a specific toxic effect on the eccrine gland. With the increasing use of the benzodiazepines, such lesions could be seen more frequently in the future.
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7/7. Case report: interferon induced coma in Sheehan's syndrome.

    A 54-year-old woman who was being treated with 10 million units (mu) of natural interferon (IFN)-alpha per day for chronic active hepatitis c at a local clinic, developed coma on the fourth day of treatment. On admission to Yamagata University Hospital, she was still in a state of semicoma with severe hyponatraemia (122 mEq/L) and hypochloraemia (89 mEq/L). After the administration of electrolytes, her condition improved remarkably. Endocrinological loading tests showed a hypofunction of the anterior pituitary gland. In consideration of these results, and her past experiences of haemorrhage during childbirth and subsequent amenorrhoea, we diagnosed her illness as a coma as a result of Sheehan's syndrome which had become overt during IFN therapy. She recovered completely after treatment with hydrocortisone and l-thyroxine.
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